Given the dynamic nature of this process and the early onset of cardiomyopathy in nesprin 1f/f;nesprin 2−/−;Nkx2.5Cre hearts, we hypothesized that loss of Nesprin 1 and/or 2 would cause morphological and positional defects in cardiomyocyte nuclei. The gene discussed is SYNE1; the disease is cardiomyopathy.